What is the role of reabsorption of HCO3- in the pathogenesis of metabolic acidosis?

Updated: Oct 10, 2018
  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN  more...
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With a serum HCO3- concentration of 24 mEq/L, the daily glomerular ultrafiltrate of 180 L, in a healthy subject, contains 4300 mEq of HCO3-, all of which has to be reabsorbed. Approximately 90% of the filtered HCO3- is reabsorbed in the proximal tubule, and the remainder is reabsorbed in the thick ascending limb and the medullary collecting duct.

The 3Na+ -2K+/ATPase (sodium-potassium/adenosine triphosphatase) provides the energy for this process, which maintains a low intracellular Na+ concentration and a relative negative intracellular potential. The low Na+ concentration indirectly provides energy for the apical Na+/H+ exchanger, NHE3 (gene symbol SLC9A3), which transports H+ into the tubular lumen. H+ in the tubular lumen combines with filtered HCO3- in the following reaction:

HCO3- + H+ ↔H2 CO3 ↔H2 O + CO2

Carbonic anhydrase (CA IV isoform) present in the brush border of the first 2 segments of the proximal tubule accelerates the dissociation of H2 CO3 into H2 O + CO2, which shifts the reaction shown above to the right and keeps the luminal concentration of H+ low. CO2 diffuses into the proximal tubular cell perhaps via the aquaporin-1 water channel, where carbonic anhydrase (CA II isoform) combines CO2 and water to form HCO3- and H+. The HCO3- formed intracellularly returns to the pericellular space and then to the circulation via the basolateral Na+/3HCO3- cotransporter, NBCe1-A (gene symbol SLC4A4).

In essence, the filtered HCO3- is converted to CO2 in the lumen, which diffuses into the proximal tubular cell and is then converted back to HCO3- to be returned to the systemic circulation, thus reclaiming the filtered HCO3-.

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